Evidence map›Paper›PMID 29875152›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2018

Evidence for the Existence of a CXCL17 Receptor Distinct from GPR35.

Nurul A S Binti Mohd Amir, Amanda E Mackenzie, Laura Jenkins, Karim Boustani, Marston C Hillier, Tomoko Tsuchiya, Graeme Milligan, James E Pease

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed, 64 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 3 countries.

Nurul A S Binti Mohd AmirInflammation, Repair and Development Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, United Kingdom.ORCID 0000-0003-1633-0365
Amanda E MackenzieCentre for Translational Pharmacology, Institute of Molecular, Cell, and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom; and.
Laura JenkinsCentre for Translational Pharmacology, Institute of Molecular, Cell, and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom; and.
Karim BoustaniInflammation, Repair and Development Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, United Kingdom.ORCID 0000-0001-9344-5890
Marston C HillierInflammation, Repair and Development Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, United Kingdom.ORCID 0000-0003-1646-7193
Tomoko TsuchiyaResearch Institute, National Center for Global Health and Medicine, Shinjuku-ku, Tokyo 162-8655, Japan.
Graeme MilliganCentre for Translational Pharmacology, Institute of Molecular, Cell, and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, United Kingdom; and graeme.milligan@glasgow.ac.uk j.pease@imperial.ac.uk.ORCID 0000-0002-6946-3519
James E PeaseInflammation, Repair and Development Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London SW7 2AZ, United Kingdom; graeme.milligan@glasgow.ac.uk j.pease@imperial.ac.uk.ORCID 0000-0003-3749-0341
Lung Institute · USUniversity of Glasgow · GBNational Center for Global Health and Medicine · JP

Funding

Biotechnology and Biological Sciences Research Council BB/P000649/1Medical Research Council G1000758
6 · The paper itself

Abstract

The chemokine CXCL17 is associated with the innate response in mucosal tissues but is poorly characterized. Similarly, the G protein-coupled receptor GPR35, expressed by monocytes and mast cells, has been implicated in the immune response, although its precise role is ill-defined. A recent manuscript reported that GPR35 was able to signal in response to CXCL17, which we set out to confirm in this study. GPR35 was readily expressed using transfection systems but failed to signal in response to CXCL17 in assays of β-arrestin recruitment, inositol phosphate production, calcium flux, and receptor endocytosis. Similarly, in chemotaxis assays, GPR35 did not confirm sensitivity to a range of CXCL17 concentrations above that observed in the parental cell line. We subsequently employed a real time chemotaxis assay (TAXIScan) to investigate the migratory responses of human monocytes and the monocytic cell line THP-1 to a gradient of CXCL17. Freshly isolated human monocytes displayed no obvious migration to CXCL17. Resting THP-1 cells showed a trend toward directional migration along a CXCL17 gradient, which was significantly enhanced by overnight incubation with PGE

Indexed as

Animalsbeta-ArrestinsCalcium SignalingChemokines, CXCChemotaxisEndocytosisHumansImmunity, InnateMiceMonocytesReceptors, G-Protein-CoupledSignal TransductionTHP-1 Cellsbeta-ArrestinsChemokines, CXCCXCL17 protein, mouseGPR35 protein, mouseReceptors, G-Protein-Coupled

Identifiers

PMID29875152
PMCPMC6036231
OpenAlexW2806449183

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.